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Disease Entity

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Disease

Blunt ocular trauma encompasses damage to ocular and extraocular structures from a non-penetrating mechanical force. Approximately two million cases of blunt ocular injury are reported annually in the United States, making blunt ocular trauma the most prevalent cause of ocular injury and the greatest contributor to monocular vision loss  (1).

The Birmingham Eye Traumatic Terminology system describes ocular blunt force trauma as either a closed or open globe injury caused by a blunt force trauma (2). Other classifications may be used to describe these injuries such as accidental or non-accidental, coup or countercoup, and direct or indirect (3).

Etiology

Blunt ocular trauma is the direct result of a blow to the globe itself or the surrounding orbital structures. The majority of blunt ocular injuries result in damage to the anterior segment only (63.5%), but damage to the orbit and posterior segment are also possible though less likely (19.2% and 1.6% respectively) (4). The degree of severity ranges from superficial damage with no effect on vision to open globe rupture resulting in permanent vision loss.

Balls and activities involving wooden sticks are the objects most frequently associated with blunt ocular injuries, especially in pediatric populations (5-7). Other injury causes include assault/beatings, chopping wood, fireworks, foam or plastic bullets, bungee cords, and exercise bands (5, 7-11).

Etiology

There are approximately 1.5-2 million cases of blunt ocular injuries reported each year in the US and are the most common type of ocular injuries worldwide (21.5-60.8%) (12-15). For pediatric populations in the US, the cost burden associated with these injuries is around $200 million a year (12). The highest demographic factors associated with blunt ocular injuries were patients ages 15-18 or >70 years old. Males make up the majority of cases with around 62.4% in pediatric populations and 83% or more in adults (4, 12, 16-19). However, the incidence of blunt ocular injuries between males and females becomes more equal for populations aged >65 years old (20). The risk for sustaining a blunt ocular injury follows a bimodal distribution with the majority of injuries occurring in patients aged <18 or >70 years old (21).

Specific etiological causes of Blunt ocular injuries vary by age. The majority of blunt ocular injuries in pediatric populations are accidental incidents that occur outdoors and in the setting of sports and recreational activities (12). For adults, the majority of incidents result from household injuries though males are more likely to sustain blunt ocular injuries from occupational hazards, automobile, and sports related injuries compared to females (8, 20). Sports related injuries, specifically basketball and soccer, are significant as they are highly associated with open globe injuries (22). With advanced age, falls become the primary mechanism for BOI which are also associated with open globe injuries (20, 23).

Seasonality is another contributor to blunt force trauma with higher prevalence of injuries occurring during summer months (4, 12).

Risk Factors

Lack of eye protection, involvement in sports, intense activities, occupations with high hazard risks (plumbing, manufacturing, and agriculture), alcohol consumption, and motorcycle use are also risk factors (5, 7, 8, 16, 22, 24). Anatomic and systemic risk factors include short axial length, Marfan's syndrome, homocystinuria, and spherophakia which may increase the severity of a blunt ocular injury (25, 26). Pediatric patients who are in the critical years of development are at an increased risk of developing amblyopia secondary to complications of blunt force trauma.

General Pathology

Pathologies associated with blunt ocular injuries are wide ranging and affect extraocular structures, the anterior segment, and the posterior segment. Extraocular pathologies include orbital fracture and extraocular muscle entrapment which are ocular emergencies requiring immediate intervention (27).

Complications associated with anterior segment damage include corneal abrasion, endothelial corneal staining, angle recession, iridodialysis, iritis, hyphema, and subluxation or dislocation of the lens (3, 11, 17, 21, 28-31).

Posterior segment injuries include vitreous hemorrhage, commotio retinae, choroidal rupture, posttraumatic macular hole, traumatic chorioretinal disruption, and scleral rupture (6, 9, 31-38). Blunt ocular injuries increase the risk of developing glaucoma due to aqueous outflow tract obstruction from angle recession, inflammation, hyphema, iridodialysis, and cyclodialysis (3, 7, 19, 21, 29, 39). Patients with sickle cell disease who suffer any degree of hyphema are more susceptible to obstruction due to increased blockage by sickled cells (17). 

Patients aged 0-6 who sustain vision loss from open globe injuries are at increased risk of developing amblyopia (6, 40).

Pathophysiology

Blunt ocular injuries cause a rapid compression and subsequent expansion of anterior-posterior forces which results in diffuse intraocular damage and bleeding from highly vascularized structures (7, 41). During compression, aqueous humor is displaced toward the iridocorneal angle potentially splitting the longitudinal and circular fibers of the ciliary body along different planes and narrowing the anterior chamber angle (7, 41). This force can avulse the iris from its natural attachment to the ciliary body (iridodialysis) (29). Zonules suspend the lens in place but are especially susceptible to straining forces causing the lens to move slightly out of its natural position (subluxation) or completely into the anterior chamber or vitreous cavity (dislocation) if damaged (5, 25, 30, 31). Shearing and compressive forces rupture highly vascularized structures such as the iris, ciliary body, and choroid resulting in hyphema or vitreous hemorrhage (7, 32). Necrotic tissue, microbic debris, and disrupted iris pigment provoke an inflammatory response and can reduce aqueous humor outflow increasing intraocular pressure (3).

Posterior segment injuries are also caused by anteroposterior compression. Macular commotio is associated with orbital floor fractures as a result of elevated intraocular pressure (IOP) from contrecoup retropulsion (9). Extramacular commotio occurs more often in an inferotemporal to temporal location and is associated with direct orbital rim fractures (9). Difference in integrity and elasticity of intraocular structures predisposes more rigid structures like the retinal pigment epithelium and Bruch’s membrane to rupture (34). Direct Blunt ocular injuries predominantly rupture parallel to the equator and along the ora serrata, whereas indirect trauma causes concentric breaks to the thickened optic nerve area (34, 42). As the wound heals, the area surrounding the tear becomes highly vascularized. This choroidal neovascular membrane often lacks endothelial tight junctions which result in exudation and increases the risk of serious retinal detachment (43). A complication of high-velocity trauma is the separation of the choroid off from the sclera (sclopetaria) due to anteroposterior compression with subsequent expansion (37, 44).

Tissue remodeling can result in fibrous tissue which invades neuro-retinal layers interfering with the integrity of the RPE (42). This results in replacement of choroid and retina with scarring causing chronic vision impairment (34, 37).

Primary Prevention

One of the most effective strategies to prevent blunt ocular injuries is wearing ocular protection like safety glasses/goggles during risky activities such as sports, chopping wood, or in hazardous occupations. Other measures such as using helmets, seatbelts, as well as working in well-illuminated areas and limiting alcohol consumption have been demonstrated to effectively prevent blunt ocular trauma (20, 22, 23). For older patients, removing household tripping hazards and utilizing moving aids like a cane or walker can prevent falls.

Diagnosis

History

A proper history will investigate the specific mechanism of injury, the time since the injury, associated symptoms such as pain, photophobia, flashes, and floaters which are all predictors of severity and vision outcome (16). It is also important to obtain patient history such as prior trauma, previous surgical interventions, medications such as anticoagulants, and systemic conditions like bleeding/coagulation disorders, Marfan’s, homocystinuria, and Ehlers Danlos. Patients at risk for sickle cell disease should be evaluated as it influences medical management (19, 25, 45).

Physical Examination

A complete ophthalmic examination is required to assess the severity of a blunt ocular injury. Special attention should be paid to the presence of enophthalmos and extraocular muscle movement as abnormalities may indicate ophthalmic emergencies (27). Presence of foreign bodies, hyphema, lens placement, and scleral integrity is also important to evaluate as prompt surgical intervention may be required (5, 18, 27, 38). The cornea should be examined with a fluorescein Seidel test to detect abrasions or full-thickness wounds that might otherwise be missed (27). Measurement of IOP is essential as prompt treatment can reduce long-term optic nerve damage (17).

If IOP is found to be elevated, further investigation with gonioscopy is warranted to assess angle recession and trabecular damage (3). If there is minimal risk of acute angle attack, a dilated fundoscopic exam should be performed to assess posterior segment damage. If this view is limited by hyphema, traumatic cataract, or vitreous hemorrhage, additional imaging is required (32).

Signs

Identifying characteristic orbital findings after a blunt ocular injury is necessary to rule out an ocular emergency. An asymmetrical eyeline with enophthalmos or exophthalmos may indicate orbital fracture while pain or restricted movement with extraocular movement may indicate muscle entrapment (27).

Most anterior segment injuries can be detected at the slit lamp while more subtle signs require additional diagnostic measures (21). Corneal abrasions and scars will appear hyperfluorescent with dye. Iritis may be detected by the presence of white blood cells in the anterior chamber and keratic precipitates (KP) on the corneal endothelium (11). Cycloplegia on exam can be a sign for ciliary body or oculomotor nerve (CN III) damage which would be associated with additional findings like ptosis and ophthalmoplegia (41). Posterior synechiae to the lens is another sign of persistent inflammation (36). Hyphema appears as a collection of blood in the anterior chamber while vitreous hemorrhage presents as a bloody obscuration of the posterior segment. On anterior chamber optical coherence tomography (AC-OCT), thickening of the nasal and temporal quadrants as well as enlargement of Schlemm’s canal is often associated with hyphema (3). Signs of lens displacement include iridodesis of the lens, vitreous prolapse in the anterior chamber, decreased anterior chamber depth, and angle closure with monocular acute IOP rise (26). On gonioscopy or AC-OCT, angle recession is indicated by posterior displacement of the iris root, exposed ciliary band, and widening of the iridocorneal angle (21).

Fundoscopy or imaging can identify signs associated with posterior segment injuries. Commotio retinae appears as transient whitening and opacification of the neuroretina and is most seen in the macular and mid-periphery regions (9, 33, 46, 47). While initially thick, OCT angiography will begin to show reduction in the ganglion cell complex thickness after 1 month with a full reduction being observed in many patients after 6 months (33). Signs of healing include increased vascularization though this can eventually result in scarring which would be seen later in the disease course (35). Choroidal ruptures are characteristically seen as yellow/white lines either parallel to the ora serrata or concentric to a thickened optic nerve (34, 42). In the acute phase, the area surrounding the rupture will appear hypofluorescent on fluorescein angiography indicating reduced perfused (34). A full-thickness wound on fluorescein Seidel test will appear as a dark "streaming" pattern where the dye is washed away by the leaking fluid (27).

Symptoms

Symptoms associated with blunt ocular injuries include pain, photophobia, immediate or progressive vision loss, diplopia, glare, halos, flashes, floaters, and redness (11, 29).

Clinical Diagnosis

The diagnosis of blunt ocular injury can be reached by integrating history with slit lamp findings. Due to the several sequelae associated with blunt force trauma, detailed investigation is required to screen for additional complications. This includes determining location and severity of trauma throughout anterior and posterior segments (12, 16).

Diagnostic Procedures

In many cases, full appreciation of blunt force trauma requires additional imaging. Computed tomography (CT) may be used to rule out orbital and facial fractures (27). OCT is useful to assess anterior chamber angle, and integrity of the trabecular meshwork, retina, and macula (3, 21). If hemorrhage occludes view, B-scan ultrasound may also be used to assess retinal damage (48). Fluorescein angiography is useful to determine choroidal involvement and post-injury scarring (34, 42).

Laboratory Test

Patients with persistent hyphema who are not currently receiving anticoagulant treatment should receive coagulation studies (CBC, PT, aPTT, INR) labs to evaluate for bleeding and coagulation disorders (45). Sickle cell may be screened with hemoglobin electrophoresis as medical management may differ for patients with this trait (19).

Differential Diagnosis

Suspected cases of blunt ocular injury should rule out foreign body penetration (27). In addition, several findings of blunt ocular injury are associated with other etiologies. For example, lens displacement can be seen in connective tissue disorders not associated with a history of trauma (25). Vitreous hemorrhage is also seen in various conditions such as diabetic retinopathy or macular degeneration. Elevated IOP can also be seen with primary open angle glaucoma, corticosteroid use, or intracranial idiopathic hypertension (IIH). Many findings of blunt ocular injury may occur without a preceding cause such as subconjunctival hemorrhage, or retinal detachment. In addition, spontaneous hyphema may result from uveitis, coagulation/bleeding disorders, various underlying pathologies that cause neovascularization such as diabetes or neovascular glaucoma (45).

Management

Management of blunt ocular injuries is dependent on severity and associated findings (40). In the acute phase post-injury, it is recommended to wear a protective eye shield over the injured eye, keep the head elevated, and to restrict activity (17). If hyphema is present, consider temporarily discontinuing anticoagulant and antiplatelet medications to reduce rebleeding and the risk of long term damage to the aqueous outflow tract (17). The exception to stopping these medications would be if the patient is at high risk of embolism or stroke.

General Treatment

Medical Therapy

In patients with angle recession or elevated IOP, medical therapy consists of IOP-lowering medications such as prostaglandin analogues, beta-blockers, and alpha-agonists (21, 49). Patients with sickle cell disease who develop hyphema require aggressive IOP management (17, 19). However, Carbonic anhydrase inhibitors should be used with caution or avoided for these patients as they can increase sickling of red blood cells (19).

If patients exhibit signs of iritis, cycloplegic administration, topical corticosteroids, and NSAIDs may be used to reduce inflammation and pain (11, 17). Corticosteroids may also be considered to accelerate hyphema resolution and reduce risk of rebleeding (18, 45).

Patients who experience neovascularization secondary to choroidal damage may benefit from the use of anti-VEGF such as bevacizumab to reduce the likelihood of long term vision loss from scarring (43).

Medical Follow-up

Patients who receive IOP-lowering medications should receive routine follow-up for pressure measurements until pressure returns to baseline (49). The contralateral non-injured eye should also be monitored as increases in the non-injured eye has been associated with post-injury rise in IOP (49).

Patients on corticosteroids should be directed to taper use gradually as tolerated to reduce flares and steroid-related complications (17).

If symptoms do not improve with medication use, further interventions or surgery may be indicated (16).

Surgery

Anterior chamber washout, trabeculectomy, peripheral iridotomy, or placement of an IOP-lowering shunt may be considered for patients with increased IOP secondary to persistent hyphema (17, 45).

Phacoemulsification, and intraocular lens placement is indicated for patients with traumatic cataracts (32). Those with lens dislocation will also benefit from pars plana vitrectomy (PPV) and a tension ring (6, 40).

Vitreous hemorrhage that does not self-resolve or significantly restricts view of the posterior segment may also benefit from PPV. PPV may also be considered earlier for children ages 0-6 who are at increased risk for amblyopia (6).

Retinal detachment requires immediate attention with surgical repair (50). This can include PPV with scleral buckle or pneumatic retinopexy.

Severe cases of blunt force trauma with open globe injury will require emergency repair occasionally requiring chorioretinectomy (38, 51).

Complications

Complications associated with blunt ocular injuries are extensive and varied. Acute complications include secondary glaucoma, iris pigment deposition, inflammation, trabecular meshwork, and ciliary body damage (3, 21, 49). If inflammation is not addressed, the risk of synechiae formation increases (36).

Late complications of blunt ocular injuries include traumatic cataract formation, elevated IOP in both eyes and permanent endothelial corneal staining from persistent hyphema (3, 16, 32, 49). Macular hole may also form following disruption in RPE integrity. Amblyopia is a special consideration among pediatric populations if vision does not improve (6, 40).

Prognosis

The most significant predictor of long-term visual outcome is visual acuity at presentation (5, 16, 22, 40, 43). Factors that are associated with favorable outcomes are early intervention, absence of posterior-segment involvement, preserved initial visual acuity, and young age. The greatest predictors of unfavorable outcomes include complete vision loss at initial presentation and scleral rupture (16, 40).

A negative prognosis is associated with different types of complications. The most significant of these include the presence of hyphema (OR of 37.6) and posterior segment involvement (OR 8.62) (12). Vitreous hemorrhage, delay to intervention may also be linked with poor outcomes. The specific mechanism of injury is another negative predictor for visual outcome. For example, injuries caused by firearms or projectiles or those associated with assault, sports, or alcohol consumption may result in long-term loss of vision (8).

Conditions that are more likely to spontaneously resolve include hyphema, vitreous hemorrhage, and flashes/floaters not associated with retinal detachment (6, 18, 19, 32, 36). Complications that require intervention to heal or prevent worsening include traumatic cataracts, angle recession or elevated IOP, retinal detachment, or ruptured globe.

Additional Resources

Please see other Eyewiki articles on orbital/facial fractures, angle recession, hyphema, secondary glaucoma, iritis/uveitis, iridodialysis, vitreous hemorrhage, choroidal rupture, retinal detachment, glaucoma management, scleral rupture, and open globe injuries.

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